Evidence map›Paper›PMID 36252128›Full record

ArticleAmerican journal of physiology. Cell physiology2022

Temporal analysis of skeletal muscle remodeling post hindlimb ischemia reveals intricate autophagy regulation.

Mattia Scalabrin, Viktor Engman, Amanda Maccannell, Annabel Critchlow, Lee D Roberts, Nadira Yuldasheva, T Scott Bowen

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. European journal of translational myology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Mattia ScalabrinSchool of Biomedical Science, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.
Viktor EngmanSchool of Biomedical Science, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.
Amanda MaccannellLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom.
Annabel CritchlowSchool of Biomedical Science, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.
Lee D RobertsLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom.ORCID 0000-0002-1455-5248
Nadira YuldashevaLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom.
T Scott BowenSchool of Biomedical Science, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.ORCID 0000-0002-1740-2474
University of Leeds · GB

Funding

Medical Research Council MR/R014086/1Medical Research Council MR/S025472/1
6 · The paper itself

Abstract

Hind limb ischemia (HLI) is the most severe form of peripheral arterial disease, associated with a substantial reduction of limb blood flow that impairs skeletal muscle homeostasis to promote functional disability. The molecular regulators of HLI-induced muscle perturbations remain poorly defined. This study investigated whether changes in the molecular catabolic-autophagy signaling network were linked to temporal remodeling of skeletal muscle in HLI. HLI was induced in mice via hindlimb ischemia (femoral artery ligation) and confirmed by Doppler echocardiography. Experiments were terminated at time points defined as early- (7 days;

Indexed as

HindlimbIschemiaMuscle, SkeletalAMP-Activated Protein KinasesAnimalsAutophagyDisease Models, AnimalFemoral ArteryMiceMice, Inbred C57BLSestrinsAMP-Activated Protein KinasesSestrinsautophagyischemiasestrinsskeletal muscle

Identifiers

PMID36252128
PMCPMC9722248
OpenAlexW4306662152

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.